Cholesterol and hair loss
Cholesterol and hair loss


Cholesterol is vital to the normal function of all human cells; it has particular importance in skin tissue and the hair follicle.  In addition to forming an essential component of cell membranes, cholesterol acts a precursor for steroid hormones such as testosterone, progesterone, estrogen and vitamin D.

Cellular cholesterol balance must be maintained within a relatively narrow concentration range to control the rates of biosynthesis, uptake and efflux.  Cholesterol metabolism plays an important role in the regulation of keratin cell membranes, the hair growth cycle and the quality and smooth feel of the hair fibre.  Maintaining cholesterol metabolism is important for the prevention of hair loss and for hair regrowth after a period of hair thinning.


A major importance of the physical state of the membrane, is the control of the polarity of the cell which is influenced by how much water can enter and leave the cell. The water permeability of keratin cells that make up the hair and skin effect the overall level of hydration of the essential components that make up the hair and skin.

High levels of cholesterol stiffen the cell membrane of the hair follicle, reducing diffusion of molecules such as oxygen, carbon dioxide and water [1].  Several studies showed changes in the lipid content and distribution were responsible for biological events that led to brittle hair and dry skin.  In addition, in dry skin of healthy persons, it was found there was a decreased expression of keratin that forms the hair cuticle, and the hair cortex occurs (Keratin 1 and Keratin 10) [2].  This lowers the protein on the protective barrier of the hair and the proteins that make up the central canal of the hair fibre.

Dry hair and skin can encourage hair loss


Cholesterol is used to make steroid hormones such as testosterone and vitamin D, as well as other products essential for cell survival.  High levels of cholesterol have been found in populations with low testosterone and low vitamin D.  Research shows a direct correlation between zinc levels and cholesterol levels [3]. Pharmacological doses of between 35 mg and 50 mg of elemental zinc have been shown to be effective in lowering cholesterol but lower doses of 15 mg (the RDA for zinc) have no noticeable effect [4].

Supplementation with increases cholesterol conversion to vitamin D and testosterone via membrane-bound transcription factor peptidase site 2.  This metalloprotease is essential for the uptake and metabolism of cholesterol within the cell.

A study conducted on 827 Italian factory workers in 1990 showed men with no hair loss had an average cholesterol level of 5.369 mmol/L, men with receding hairlines had an average cholesterol level of 5.387 mol/L and men with more severe hair loss had an average cholesterol level of 5.521 mol/L.

The central finding of another study [5], was the excess of cholesterol within the hair follicle niche can trigger an innate immune response that leads to the induction of Toll-like receptor and Interferon gamma gene expression.  This leads to the activation and recruitment of T cells and macrophages that surround the hair follicles and initiates an inflammatory response resulting in the hairless lesions seen in alopecia areata.

Hair loss associated with abnormal cholesterol metabolism is also seen in women with low, normal or high levels of cholesterol. It appears the ratio of high density lipoproteins compared to low density lipoproteins is the factor that affects hair growth.

Cholesterol and hair loss


Cholesterol is insoluble in water and needs to be transported by lipoproteins in the blood. There are two main types of cholesterol protein carrier: high density lipoprotein (HDL) and low-density lipoprotein (LDL).  HDL is known as “good cholesterol because this lipoprotein transports cholesterol to your liver to be expelled from the body.  LDL is known as “bad cholesterol” because it transports cholesterol throughout the body. These definitions are somewhat arbitrary as good and bad is defined only by direction of transport.

Arguably, a lower level of HDL could demonstrate functional use of cholesterol by the conversion to other products.  By this standard, high HDL would become “bad” as it shows lack of utilisation by the body and high LDL would be seen as “good” as it shows the starter materials are available and there is a secondary issue inhibiting cholesterol metabolism.  This theory is supported by the fact that high levels of HDL can be seen in patients that have previously had a heart attack.  High levels of HDL are linked to other conditions including thyroid disorders, alcohol consumption and inflammatory disease.

The ratio of HDL to LDL is significantly linked to hair loss, this further suggests the invalidity of the “good vs bad” determination.  Doctors calculate an individual’s cholesterol ratio by dividing their total cholesterol by their HDL. The optimal ratio is between 1 and 3.5, a higher ratio is linked to an increased risk of hair loss.

This ratio determination demonstrates HDL and LDL by itself cannot be taken as a negative or positive value as a 1:1 ratio of HDL and LDL is a more significant predictor of potential hair health than the individual measurements of either.

HDL and LDL levels influence hair loss


Vitamin D is linked to cholesterol because we use the cholesterol in the epidermal cells that make up the skins to make vitamin D from sunlight. The vitamin D is later transformed again in the liver and kidneys, but cholesterol is required for the first step.

Vitamin D is involved in cell growth, the reduction of inflammation, glucose metabolism and immune function.  At the start of a normal hair growth cycle, stem cells migrate from the hair follicle bulge and are stimulated to grow and differentiate in the germinal matrix forming the seven inner layers of the hair fibre.  Differentiation is a process by which stem cells change and grow into a more specialised cell type through a succession of alterations in cell morphology, metabolic activity and responsiveness to signals.

Vitamin D mediates the differentiation of epidermal cells and a lack of vitamin D leads to decreased interfollicular cell differentiation.  Cells that are not able to develop as normal, are not able to become part of the hair fibre matrix and lie dormant in the epidermal layer of the skin. Whilst the exact mechanisms that control the stem cell response to low levels of vitamin D are unclear, low levels of vitamin D are linked to non-scarring alopecia, alopecia areata and androgenic alopecia in women.

Vitamin D is associated with hair loss at levels below 75 mol/L (30 ng/mL).

nmol/L ng/mL
Less than 30 Less than 12 Vitamin D deficient.
30-50 12-20 Considered to be inadequate for overall health.
50-75 20-30 Considered to be adequate for bone health and overall health.
75-125 30-50 Optimal levels for healthy hair growth.


Balancing cholesterol levels will help with new hair growth and will reduce the severity of current hair loss. If you are worried that your hair loss may be due to an unbalanced lipid profile talk to your doctor and request a lipid profile that will cover triglycerides, HDL, LDL HDL/LDL ratio and total cholesterol.  Checking vitamin D levels can also help determine if you are not metabolising cholesterol optimally.


  1. Contribution of membrane cholesterol to outer hair cell lateral wall stiffness. Otolaryngology—Head and Neck Surgery119(1), pp.14-20.
  2. Effects of xerosis and ageing on epidermal proliferation and differentiation. British Journal Dermatology, 137 (1997), pp. 219-225
  3. Relationship between the nutritional status of zinc and cholesterol concentration of serum lipoproteins in adult male rats. The American journal of clinical nutrition34(11), pp.2376-2381.
  4. Age-Related Eye Disease Study Research Group, 2002. The effect of five-year zinc supplementation on serum zinc, serum cholesterol and hematocrit in persons randomly assigned to treatment group in the age-related eye disease study: AREDS Report No. 7. The Journal of nutrition132(4), pp.697-702.
  5. Sterol intermediates of cholesterol biosynthesis inhibit hair growth and trigger an innate immune response in cicatricial alopecia. PloS one7(6), p.e38449.